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We incidentally observed an accumulation of un-secreted FLP-7mCherry protein in the ASI neurons of unc-31 mutants (not shown).
Both ΔdevR (Fig. 1) and ΔdevSΔdosT double mutants (not shown) were unresponsive confirming that the response to AA was mediated through the DevRS/DosT signaling pathway.
Consistent with our prior studies [6], no measurable differences in cell survival were observed in the presence or absence of WT CRT or its mutants (not shown).
In support of this, Lhp1 mutants where 8 residues in either RNP1, RNP2, or both RNPs are replaced with alanine are mislocalized in pse1-1 but not Δkap108 or different Kap mutants (not shown).
Similar phenotypes were observed with ΔnifD mutants (not shown).
However, mGluR and Homer levels appeared unaltered in drep-2 mutants (not shown).
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There were no significant changes in D-CaM fluorescence emission upon addition of the helix B S511D mutant (not shown, see41,44).
In IF microscopy with TB5, no fluorescent signal was obtained with Ad5F497D mutant (not shown).
Production of each Ssp4 mutant (Fig. 1B) or rSsp4 mutant (not shown) was demonstrated by Ssp4 Western blotting.
As it is shown above, hSpry2 Y55F mutant was unable to inhibit cyP-induced ERK/Elk1 pathway activation, whereas hSpry2 P59A P304A double mutant (and hSpry2 P59A single mutant, not shown) showed a potent inhibitory effect (Fig. 1 and 2B).
While we confirmed the circular muscle defects in the Shh mutant (Fig. 3F), we did not find such a defect in the Ihh mutant (not shown; see Discussion).
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